Onkologie. 2012:6(4):208-213

Biological therapy of chronic myeloid leukemia

Elena Tóthová, Adriana Kafková

Ústav klinickej a lekárskej biofyziky UPJŠ, Košice

Klinika hematológie a onkohematológie UN L. Pasteura a UPJŠ, Košice

The phenomenal success of therapy with tyrosine kinase inhibitors (TKI) in Philadelphia chromosome (Ph) – positive chronic myeloid

leukemia (CML) has dramatically changed the prognosis of this disease. Despite the fact that first-line therapy of CML using imatinib

represents revolutionized the treatment of this disease, it became clear that during 5 years 25–35 % of the patients require change

in the therapy due to the development of imatinib resistance or failure. The most frequent mechanism responsible for imatinib resistance

is development of mutation in BCR-ABL kinase domain. Mutations cause different level of imatinib resistance and while some of them

can be overcome by increased dose of imatinib, others seem to be resistant to nilotinib and others are more resistant to dasatinib. This

review is focused on primary treatment and treatment after imatinib failure. It has been shown recently that advances in molecular

methods enable to better understand disease itself, weight benefit to risk ratio of the therapy, individualize therapeutic approach and

eventually adjust CML therapy earlier in order to minimize the risk of CML progression to accelerated phase.

resistance, new drugs.

Keywords: chronic myeloid leukemia, tyrosine kinase inhibitors, imatinib, dasatinib, nilotinib, BCR-ABL domain mutations, imatinib

Published: October 1, 2012  Show citation